The purpose of the study was to establish pathogenetic mechanisms, in particular, disorders of purine and protein metabolism of blood serum, which can cause increased susceptibility of gout patients to periodontal diseases, contribute to their progression and mutually burden the course of both diseases, which is a necessary prerequisite for effective prevention and treatment of these patients. Materials and methods. A biochemical study of venous blood was carried out in 60 men with gout, aged 30 to 59 years, who were undergoing inpatient treatment in the rheumatology department of Lviv Regional Clinical Hospital. All the examined were men, which is related to the gender-age characteristics of the prevalence of gout. 2 observation groups were formed: the main group consisted of 30 patients with generalized periodontitis on the background of gout; the comparison group included 30 people with generalized periodontitis, not burdened by rheumatological pathology. The results were compared with the indicators of 20 conditionally healthy individuals (control group). The research was carried out in the period between attacks of gouty arthritis, two weeks after therapy with non-steroidal anti-inflammatory drugs. In order for the test results to be objective, 24 hours before blood sampling, patients were recommended to exclude fruit and vegetable juices, caffeine, and alcoholic beverages from their diet, as well as to limit physical and mental exertion. Results and discussion. The results of the research presented the following: the patients of the main group had the highest level of the main marker of purine metabolism – uric acid in blood serum; it was 0.62 ± 0.18 mmol/l with a normal reference range of 0.20 - 0.42 mmol/l. In the comparison group, the laboratory indicator of uric acid content in blood serum was 0.38 ± 0.09 mmol/l and was at the upper limit of reference values, but it was by 1.6 times lower than in the main group, p < 0.05. In the control group, the lowest level of uric acid was observed with a digital value of 0.26 ± 0.06 mmol/l, which was by 1.5 times less than in the control group and by 2.4 times less compared to the data of the main group, p < 0.01. The level of urea, a marker of protein metabolism, in patients with generalized periodontitis on the background of gout was 9.21 ± 2.24 mmol/l and was by 1.3 times higher than the similar indicator of persons not burdened by rheumatological pathology (6.89 ± 1.53 mmol/l, p < 0.01) and by 1.9 times higher than in healthy individuals (4.72 ± 1.08 mmol/l, p < 0.01). Conclusion. According to the results of a biochemical study of the blood serum of patients with generalized periodontitis associated with gout, a significant increase in the concentration of uric acid was established, which indicated a violation of purine metabolism in these patients. Also, in patients with periodontal pathology on the background of gout, violations of protein homeostasis were observed, which was indicated by a high level of urea in the blood serum. Such a situation may indicate the presence, both at the systemic level in general and in periodontal tissues, in particular, of deep destructive processes that affect nuclear structures rich in nucleic acids, and the existence of a correlation between hyperuricemia and the destructive-inflammatory process in periodontics. Violations of purine and protein homeostasis contribute to the progression and mutually burden the course of both diseases
Keywords: generalized periodontitis, gout, blood serum, uric acid, urea
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